IndraLab

Statements



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"Taken together, these findings indicated that UCHL1, negatively regulated by Sp1, promoted H O -mediated cell injury, oxidative stress, apoptosis and senescence, and modulated NF-κB signaling in HEI-OC1 cells."

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"In this context, PEM treatment may induce senescence in NSCLC cells XREF_BIBR, however, it is possible that UCHL1 levels could be increased in senescent cells, thereby modifying the senescence process XREF_BIBR."

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"Overexpression of UCHL1 was found to induce senescence, likely due to increased production of p14ARF, p53, p27KIP1 and decreased MDM2 levels [XREF_BIBR]."

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"This effect of UCHL1 on NF-κB signaling was abrogated by Sp1 overexpression.In conclusion, the present study suggested that UCHL1, negatively regulated by Sp1, could promote H O -mediated cell injury, oxidative stress, apoptosis and senescence and inhibit NF-κB signaling in an in vitro model of ARHL."

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"In addition, UCHL1 overexpression enhanced cell viability and promoted oxidative damage, apoptosis and senescence in H 2 O 2 -induced HEI-OC1 cells."

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"Indeed, we could observe more cells with an increased level of SA-beta-gal in cells overexpressing UCHL1 compared to the respective mock control cells, suggesting that the overexpression of UCHL1 leads to the induction of cellular senescence in LNCaP prostate cancer cells."